Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042875 (vitamin E deficiency)
 916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Concentrations of alpha-tocopherol (alpha-T) in plasma, cerebrum, cerebellum, midbrain and brain stem and activity of selenium (Se)-dependent glutathione peroxidase (GSH-Px) in plasma were measured in 1- and 15-month-old male F344 rats fed diets containing vitamin E (E, IU/kg) and Se (ppm) in the following combinations: 30 E, 0.1 Se (control diet, minimum requirements); 200 E, 0.2 Se; 0.0 E, 0.2 Se; 200 E, 0.0 Se; 0.0 E, 0.0 Se for 8 or 20 weeks. alpha-T and GSH-Px levels in plasma were reflective of dietary treatment in young rats in which an interaction of the two nutrients was noted. A longer period of dietary vitamin E deficiency was necessary to deplete plasma alpha-T and depress GSH-Px activity significantly in the old rats. Among the brain regions of all ages, cerebrum and midbrain had the highest concentrations of alpha-T while cerebellum showed the lowest. However, cerebellum of young rats and cerebellum and brain stem of old rats had a greater alpha-T accumulation with doubly supplemented diets, whereas only cerebellum of young and old rats showed a marked increase of alpha-T with vitamin E supplementation. In old rats, vitamin E deficiency resulted in greater depletion of alpha-T in cerebellum and brain stem than cerebrum and midbrain regions. Se deficiency in brain stem of young and old rats significantly decreased alpha-T accumulation by vitamin E supplementation. Se supplementation marginally alleviates vitamin E depletion in brain.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Influence of dietary vitamin E, selenium and age on regional distribution of alpha-tocopherol in the rat brain. 382 94

Feeding a basal diet free of vitamins E and C to weanling male rats for 8 months resulted in biochemical changes characteristic of vitamin E deficiency. These included increased liver thiobarbituric acid values; decreased blood GSH levels, plasma vitamin E levels, and glutathione peroxidase activities; and increased activities of plasma pyruvate kinase, glutamic-oxaloacetic transaminase, creatine kinase, lactic dehydrogenase, and malic dehydrogenase. Tube-feeding vitamin C for 21 days resulted in partial reversal effects on the above parameters except activities of glutathione peroxidase, lactic dehydrogenase, and malic dehydrogenase. The results suggest that vitamin C may spare in part the metabolism of vitamin E through its antioxidant property.
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PMID:Vitamin C partially reversed some biochemical changes produced by vitamin E deficiency. 382 80

Preliminary experiments confirmed the work of others showing that the total glutathione peroxidase (GSH-px) activity of rat liver supernatant fraction may be resolved into two peaks of activity (peaks I and II) by gel filtration, and that peak I is the selenium-containing enzyme and peak II is another peroxidase indistinguishable from glutathione S-transferase (GST). In selenium and vitamin E deficiency, the total activity of the GSH-px became very low, and the total activity of GST with 1-chloro-2,4-dinitrobenzene (CDNB) as substrate was enhanced. Study of the time course of these changes as deficiency progressed indicated that the stimulus for the rise in GST (CDNB) activity was the fall in GSH-px activity which preceded it. The peroxidase activity of GST was found to reside only in the GST AA, B and B2 forms of the enzyme, which were shown to be respectively a homodimer of the Yc subunit, a homodimer of the Ya subunit and a heterodimer of the YaYc subunit. As vitamin E and selenium deficiency progressed, the B2 and AA forms of the enzyme showed enhanced activity, which was interpreted as implying that the Yc subunit of the enzyme becomes enriched as a consequence of the withdrawal of selenium from the animal's diet. Densitometric measurements of the Yc and Ya subunits confirmed that the amount of the Yc subunit was nearly doubled in selenium deficiency, relative to the Ya subunit.
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PMID:The glutathione S-transferases in selenium and vitamin E deficiency. 400 1

Selenium deficiency and vitamin E deficiency both affect xenobiotic metabolism and toxicity. In addition, selenium deficiency causes changes in the activity of some glutathione-requiring enzymes. We have studied glutathione metabolism in isolated hepatocytes from selenium-deficient, vitamin E-deficient, and control rats. Cell viability, as measured by trypan blue exclusion, was comparable for all groups during the 5-h incubation. Freshly isolated hepatocytes had the same glutathione concentration regardless of diet group. During the incubation, however, the glutathione concentration in selenium-deficient hepatocytes rose to 1.4 times that in control hepatocytes. The selenium-deficient cells also released twice as much glutathione into the incubation medium as did the control cells. Total glutathione (intracellular plus extracellular) in the incubation flask increased from 47.7 +/- 8.9 to 152 +/- 16.5 nmol/10(6) selenium-deficient cells over 5 h compared with an increase from 46.7 +/- 7.1 to 92.0 +/- 17.4 nmol/10(6) control cells and from 47.7 +/- 11.7 to 79.5 +/- 24.9 nmol/10(6) vitamin E-deficient cells. This overall increase in glutathione concentration suggested that glutathione synthesis was accelerated by selenium deficiency. The activity of gamma-glutamylcysteine synthetase was twice as great in selenium-deficient liver supernatant (105,000 X g) as in vitamin E-deficient or control liver supernatant (105,000 X g). Hemoglobin-free perfused livers were used to determine the form of glutathione released and its route. Selenium-deficient livers released 4 times as much GSH into the caval perfusate as did control livers. Plasma glutathione concentration in selenium-deficient rats was found to be 2-fold that in control rats, suggesting that increased GSH synthesis and release is an in vivo phenomenon associated with selenium deficiency.
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PMID:Effect of selenium deficiency and vitamin E deficiency on glutathione metabolism in isolated rat hepatocytes. 612 15

Vitamin E and selenium statuses were studied in thalassemic children in comparison with 16 normal controls. Twelve Hb H disease, 46 beta-thal/Hb E and 7 beta-thal major patients had lower plasma vitamin E level than controls but plasma vitamin E/total lipids ratio of Hb H disease subjects was not different from normal. Twelve Hb H disease and 33 beta-thal/Hb E patients had normal RBC Se but increased RBC GSH-Px activity. Ten vitamin E-deficient thalassemic subjects had been supplemented with 200 mg of oral vitamin E for 4-8 weeks. After supplementation, their plasma vitamin E increased and H2O2 hemolysis decreased to normal values. Their RBC GSH-Px activity also decreased but hematocrit did not change significantly. The results demonstrate that some types of thalassemic patients have vitamin E deficiency and support that vitamin E and selenium have related functions in the prevention of RBC oxidation. Vitamin E supplementation increased RBC resistance to oxidative damage.
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PMID:Vitamin E status, glutathione peroxidase activity and the effect of vitamin E supplementation in children with thalassemia. 782 84

The activities of glutathione peroxidase (GSH-Px), glutathione reductase (GSSG-R), superoxide dismutase (SOD) and the contents of malondialdehyde (MDA) and free radicals were measured, and the morphological changes were observed in the lens of control rats, selenium-deficient (SeD) and/or vitamin E deficient (VED) rats. The activities of GSH-Px in the lens of SeD rats decreased significantly. The GSH-Px activities of lens were positively related to erythrocytes selenium level. There was a free radical at g = 2.0015 in the rat lens of all groups, but the content of free radicals in the lens of SeD group was significantly higher than that of the control group. The free radical content of lens was negatively related to erythrocytes selenium level, as well as the GSH-Px activities in the lens. In vitro, ultraviolet radiation caused the generation of another kind of free radical (g = 2.0097) in the lens of all groups, but the amount of the free radical in the lens of the SeD group was also significantly higher than that of the control group. The activities of SOD and GSSG-R in VED rat lens were significantly decreased. The amount of MDA in the lens of SeD and/or VED rats were significantly increased. The results showed that the decrease of antioxidative capability in the lenses of SeD and/or VED rats accelerated the lipid peroxidation and generation of free radicals. Although only early morphological changes in SeD and/or VED rat lens were observed, it is considered that selenium and vitamin E deficiency may be involved in the occurrence of cataract.
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PMID:Biochemical and morphological changes in the lenses of selenium and/or vitamin E deficient rats. 794 5

The effects of vitamin E deficiency on diaphragm function were studied at rest and after resistive breathing (RB) in Sprague-Dawley rats (wt 300-400 g). The animals were pair fed a vitamin E-deficient diet (E-def) or a matched vitamin E-sufficient diet (E-suf). Each diet group was then further subdivided into a group that breathed unimpeded (control) and a second group that breathed through an inspiratory resistor until the animals were unable to sustain 70% of their maximum airway pressure. Diaphragm samples were obtained for analysis of thiobarbituric acid-reactive substances, glutathione (GSH) concentrations, and glutathione disulfide (GSSG) concentrations. In vitro isometric contractile studies were also performed and included twitch (Pt) and maximum tetanic (Po) tensions, force-frequency curves, fatigue index, and recovery index. Pt was significantly reduced in the E-suf RB group as well as both of the E-def groups. Po was also significantly reduced in both E-def groups. The E-def rats subjected to RB showed a significant decrease in tension at both high and low frequencies compared with the E-suf rats. Concentrations of diaphragm thiobarbituric acid-reactive substances were significantly increased in both E-def groups. RB in both E-suf and E-def rats resulted in increases in diaphragm concentrations of GSSG and decreases in the GSH/GSSG ratios. We conclude that reduction of contractile function, lipid peroxidation, and activation of the GSH redox cycle occur with RB and that these effects are significantly increased in the presence of vitamin E deficiency.
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PMID:Diaphragmatic function after resistive breathing in vitamin E-deficient rats. 844 2

Dietetic microangiopathy ("mulberry heart disease") is a common disease of weaned pigs in several countries. It is characterised by sudden death and has been associated with vitamin E deficiency. We investigated whether it could be induced by depleting pigs of vitamin E with or without a mild peroxidative challenge. In a 2 x 2 experiment, the effect on pigs of depletion of alpha-tocopherol and supplementation with alpha-tocopherol-stripped corn oil were investigated. Although dietetic microangiopathy was not induced, there was evidence of lipid peroxidation, as judged by increased concentrations of Fe++(-)induced 4-hydroxynonenal (4-HNE) and decreased amounts of linolenic acid (C18:3, omega-3) in tissue. Reduced glutathione (GSH) can conjugate to 4-HNE in an attempt to detoxify this highly toxic compound. GSH concentrations were decreased in skeletal muscle, but not in heart, of pigs that were depleted of alpha-tocopherol with or without supplementation with corn oil. The activity of glucose-6-phosphate dehydrogenase (G6PDH) was higher in heart than in skeletal muscles. It is postulated that sufficient NADPH may be produced in heart to maintain GSH concentrations at a level sufficient to conjugate the excess 4-HNE produced by alpha-tocopherol deficiency and/or oil supplementation.
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PMID:Feeding corn oil to vitamin E-deficient pigs increases lipid peroxidation and decreases tissue glutathione concentrations. 882 97

The hepatic and pulmonary effects of nitrofurantoin (40 mg/kg, intraperitoneally) were determined at 4 and 24 hr following its administration in mice fed for 10 weeks with a vitamin E sufficient, deficient or enriched diet. Liver glutathione (GSH) was reduced by nitrofurantoin at 4 hr but was unchanged 20 hr later. Nitrofurantoin did not affect liver glutathione peroxidase, glutathione reductase or superoxide dismutase activities. Liver catalase activities were decreased by nitrofurantoin at 4 hr. Lung GSH levels were increased whilst glutathione peroxidase activity was decreased at 4 and 24 hr. Lung glutathione reductase activity was reduced in certain groups. Nitrofurantoin did not affect lung superoxide dismutase, but catalase was decreased at 24 hr. Liver malondialdehyde levels were increased by nitrofurantoin in the vitamin E deficient group whilst lung malondialdehyde levels remained unchanged. Both liver and lung malondialdehyde levels were unaffected by vitamin E supplementation when compared to the vitamin E-sufficient group. These results suggest that nitrofurantoin (40 mg/kg) was deleterious to the liver and lung. Nitrofurantoin-induced lipid peroxidation was seen in vitamin E deficiency but an increase in dietary vitamin E content did not provide additional protection compared to the recommended daily allowance. The antioxidant activities of alpha-tocopherol and gamma-enriched tocotrienol were similar.
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PMID:Nitrofurantoin-induced hepatic and pulmonary biochemical changes in mice fed different vitamin E doses. 900 Feb 62

A novel creatinine metabolite, creatol (5-hydroxycreatinine), is a key precursor in the synthesis of the uremic toxin methylguanidine (MG). Creatinine is converted to creatol within the mammalian body and this conversion is mediated specifically by hydroxyl radicals. We investigated the production of creatol and MG from creatinine in rats with renal failure induced by the lipid peroxide produced as a consequence of vitamin E deficiency and depletion of the reduced form of glutathione (GSH). In addition, we examined serum levels of other guanidino compounds, namely guanidinoacetic acid (GAA) and guanidinosuccinic acid (GSA). The injury to kidneys induced by the depletion of GSH in combination with vitamin E deficiency caused markedly elevated serum levels of creatol, MG and GSA and decreased serum GAA. The molar ratio of creatol to creatinine in the serum, which should be an index of the oxygen stress mediated by hydroxyl radicals, increased with time. Therefore, the enhanced production of creatol in vitamin-E-deficient rats that have been depleted of GSH might be due to the enhanced production of oxygen radicals in this system.
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PMID:Changes in serum levels of creatol and methylguanidine in renal injury induced by lipid peroxide produced by vitamin E deficiency and GSH depletion in rats. 904 46


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